Low-dose Light Therapy on Host Immune Response: Physiological Effects and Mechanisms of Action

Abstract

The effect of low-dose light (LDL) therapy, commonly using red and near infrared (NIR) light (600-1 100 nm), has gained attention in recent years as a relatively noninvasive technique in modulating the tissue metabolic system, nervous system, blood circulation system and immune system. The progress in the basic science fields of bioenergetics and photobiology has propelled LDL into the therapeutic revolution. The immune cells including macrophages, mast cells, neutrophils and lymphocytes as responder cells by LDL have been studied in the animals and humans with producing cytokines and protective proteins. The paper will review the mechanisms of immune action of LDL at the molecular, cellular, and tissue levels on mammalian.

Full text

Low鄄doseLightTherapyonHostImmuneResponse:
PhysiologicalEffectsandMechanismsofAction
*
CHANGHao-Cai
1)
,ZHANGZhen-Zhen
2)
,LIULei
1)**
(
1) MOEKeyLaboratoryofLaserLifeScience&InstituteofLaserLifeScience,CollegeofBiophotonics,
SouthChinaNormalUniversity,Guangzhou
510631,China;
2) InstituteofHumanVirology,ZhongshanSchoolofMedicine,SunYat
-
senUniversityNorthCampus,Guangzhou
510080,China)
Abstract Theeffectoflow-doselight(LDL)therapy,commonlyusingredandnearinfrared(NIR)light(600-1100nm),hasgained
attentioninrecentyearsasarelativelynoninvasivetechniqueinmodulatingthetissuemetabolicsystem,nervoussystem,blood
circulationsystemandimmunesystem.TheprogressinthebasicsciencefieldsofbioenergeticsandphotobiologyhaspropelledLDL
intothetherapeuticrevolution.Theimmunecellsincludingmacrophages,mastcells,neutrophilsandlymphocytesasrespondercellsby
LDLhavebeenstudiedintheanimalsandhumanswithproducingcytokinesandprotectiveproteins.Thepaperwillreviewthe
mechanismsofimmuneactionofLDLatthemolecular,cellular,andtissuelevelsonmammalian.
Keywords Low-doselight,inflammatoryreaction,lymphedema,oropharyngealmucositis,radiationdermatitis,anti-infectionand
anti-tumor
DOI:10.16476/j.pibb.2017.0275
*ThisworkwassupportedbygrantsfromTheNationalNaturalScience
FoundationofChina(61361160414,31470072,61405061)andtheNatural
ScienceFoundationofGuangdongProvince,China(2014A030313419).
**Correspondingauthor.
Tel:86-20-85211436,E-mail:liulei@scnu.edu.cn
Received:July13,2017Accepted:October19,2017
生物化学与生物物理进展
ProgressinBiochemistryandBiophysics
2017,44(12):1074~1082
www.pibb.ac.cn
Since1960s,Mester
[1]
discoveredthebiological
effectsoflow-doselight(LDL)actingonbiological
tissue,LDLhadgainedattentionbymoreandmore
researchersasanovelscientificapproach,which
inducednonthermalandnondestructivebiological
reactions,fortherapeuticapplicationsinavarietyof
experimentalconditions.Patients,researchersand
cliniciansaroundtheworldaredevotingattentionto
thepotentialtherapeuticapplicationsofLDLin
immunityandothermedicalfieldsthathave
traditionallyhadalimitedtherapeuticcontributionto
patientcare.
Recently,theuseofLDLhasextendedbeyond
therealmsofwoundhealingandpain,andrecent
researchsupportsitspotentialapplicationsin
neurodegenerativediseases
[2
-
3]
,type2diabetes
[4]
,
osteogenicdifferentiation
[5]
andthrombocytopenia
[6
-
7]
.
However,theexactmechanismsofthoseeffects
inducedbyLDLarepoorlyunderstood,butthe
mechanismisprobablytobephotochemicallyrelated.
Karu,apioneerintheLDLfield,proposedthat
cytochromecoxidase(CcO)wasthephotoacceptor
andsignaltransducer
[8
-
9]
,whichaffectedthe
mitochondrialelectrontransportsystem
[10]
andthe
biologicalregulationofreactiveoxygenspecies
(ROS)
[11
-
14]
,adenosinetriphosphate(ATP)
[15]
,nitric
oxide(NO)
[16
-
17]
andintracellularCa
2+[18
-
19]
,andfurther
affectedtheailmentprocessincludinginflammation
andcytokineandgrowthfactorrelease(Figure1).The
articlesummarizestheavailableliteratureon
molecularmechanismsoftheprotectiveorenhancing

常好才,等：低功率光照疗法对机体免疫应答的影响
2017;44(12)
1ReducedinflammatoryreactionbyLDL
1.1 LDLregulatesthesecretionofcytokines
Inflammatoryreactionisthephysiological
reactioncausedbythestimulationoftrauma,bleeding
orpathogeninfection.Itistheinnateimmune
defensivereactionofimmunecellsandinflammatory
factors.Overtheyears,severalstudiesonhumansand
animalshaveshownthatLDLhasmodulatoryeffects
oninflammatorymarkersofIL-1茁,IL-6,IL-8,TNF-琢
andprostaglandinE2(PGE2),andrelievesthe
inflammatoryprocess(edema,necrosis,neutrophilcell
influx,hemorrhagicformation).AccordingtoChang
etal.
[20]
,inflammatorysymptomsarecausedbypro-
inflammatorycytokines,suchasIL-1茁,IL-6and
TNF-琢.StudybydeAlmeidaandcolleagues
[21]
reportedLDLsignificantlydecreasedtheinflammatory
mediatorlevelsofIL-1茁,IL-6andTNF-琢inacute
skeletalmuscleinjury.Similarly,LDLcouldreduced
thosecytokineproductioninthepathophysiologyof
osteoarthritis(OA)
[22]
.25J/cm
2
LDLalsodecreasedthe
levelofpro-inflammatorycytokinesofTNF-琢,IL-1茁,
andIL-8inrheumatoidarthritissynoviocytes
[23]
.
Additionally,thetrauma-inducedpro-inflammatory
stateassessedbyIL-6andIL-10waspreventedLDL
[24]
.
Inparallel,LDLpreventedtrauma-inducedreduction
inBDNFandVEGF,vascularremodelingand
fiber-proliferatingmarkers.Morerecently,LDLhas
beenshownveryinterestingeffectsonmodulation
ofcyclooxygenase2(COX-2).(880 依10)nmLDL
decreasedtheinflammatorycellinfluxandmRNA
levelsofCOX-2justininitialphaseof Achilles
tendinitis
[25]
.COX-2mRNAexpressionswerealso
significantlydecreasedbytreatmentwith904nm
LDL
[26]
.Almeida etal
[27]
.alsofoundthat904nmLDL
in1.0Jgroupsignificantlydecreasesskeletalmuscle
effectsofLDLinanumberofpathogenicconditions
includinginflammatoryreaction,cancertherapy-
inducedcomplications(lymphedema,mucositisand
dermatitis),andanti-infectionandanti-tumoreffects.
Fig.1 ThemechanismmodelofLDL
Schematicdiagramshowstheredornearinfrared(NIR)lightisabsorbedbythephotoacceptors(e.g.cytochromecoxidase)localizedinmitochondria.
Duringtheprocess,ROSandATPproductionareincreased,NOisreleased,andintracellularCa
2+
concentration([Ca
2+
]
i
)iselevated.Theseresponses
mayultimatelyleadtochangesincellmorphologyandfunction
via
activatingsometranscriptionfactors[e.g.,nuclearfactor-
资
B(NF-
资
B),hypoxia
induciblefactor-1(HIF-1),activatorprotein-1(AP-1)andcAMP-responseelementbindingprotein(CREB)].
ROS
ATP
NO[Ca
2+
]
i
Messenger
Red/NIRlight
Nucleus
Cellmembrane
CREB
AP-1
HIF-1
NF-
资
B
Genetranscription
Cytokineandgrowthfactorproduction
Extracellularmatrixdeposition
Cellproliferation,migrationandadhesion
1075· ·

生物化学与生物物理进展 Prog.Biochem.Biophys. 2017;44(12)
damagethroughlessCOX-2-derivedgeneexpression.
However,theprecisemechanismbywhichlight
affectsthecytokinesisnotyetknown.LDLprobably
modulatedthepro-inflammatorycytokinesbyreducing
theIL-1茁andCOX-2mRNAexpressionand
consequentlyreducedPGE2levelsbyreducingcell
migrationandthequantityofmacrophages,
neutrophils,andmastcellsintheinjuredtissue
[28
-
29]
.
Macrophagesandmastcellssecretethecytokineof
IL-1茁,whichinturnrecruitsCOX-2,anenzymewhich
convertsarachidonicacidintoPGE2
[30
-
31]
.Fromthe
aboveweseethatreducedinflammatoryreactionby
LDLmaydependnotonlyonthelightirradiation
parameters(wavelength,radiationdose),butalsoon
pathologicalconditionofthestudymodel.
1.2 LDLincreasesMMPsandPAactivity
Matrixmetalloproteinases(MMPs),whichare
consideredtodegradethecomponentsofthecomplex
extracellularmatrix,andplasminogenactivator(PA),
whichisimplicatedintheplasminogen-plasmin
proteolyticsystem,playakeyroleinextracellular
matrixdegradation,synthesisofkininandfibrinolysis
intheprocessofinflammation.Both660nmand780nm
verifiedbyCuryandcolleaguescoulddecreaseMMP2
activityinamodelofischemicskinflapinrats
[32]
.
AndMMP9activitywasdecreasedoninducedarthritis
inthetemporomandibularjointwith830nmLDL
treatment
[33]
.Additionally,severalhumanandanimal
studieshaveshownthatLDLwithredtoinfrared
wavelengthsreducesthereleaseofPA
[34
-
35]
.Thus,LDL
probablymodulatesPAactivitytodegradecell
adhesivemoleculesandextracellularmatrixproteins
[36]
throughactivationofMMPs
[37]
.Furthermore,
plasminogenactivatesthekinincascade via converting
prekallikreinintokallikrein
[38]
.
1.3 LDLmodulatestheimmunecellactivity
LDLalsomodulatestheactivityofmastcells,
macrophages,neutrophilsandlymphocytestoreduce
theinflammatoryprocess.RedLDLhasbeenshownto
inducethemast-celldegranulation
[39
-
40]
,leadingtothe
releaseofamultiplechemicalmediators(VEGF121,
VEGF165,VEGF189andVEGF206)
[41]
,whichare
relatedtovasodilationandvascularproliferation,and
canoptimizetheinflammatoryprocess
[42]
.Song etal.
[43]
reportedthatinratsLDLalteredthemacrophage
polarizationfromM1statetoM2state,whichdampens
theinflammatoryandadaptiveTh1responses
[44]
.Other
studiesobservedthatLDLreducedintheabsolute
numberofmacrophagesandneutrophilscompared
withtheinjurygroup
[22,45]
,resultingindecreaseof
secretionofpro-inflammatorycytokinesandenzymes
suchasIL-6andTNF-琢involvedindrivingthe
inflammatoryresponse
[46]
.Forlymphocytes,LDLcould
activatedirectlyitsproliferation invivo
[47
-
49]
,leadingto
secreteanti-inflammatorycytokineofIL-10,which
inhibitedtheproductionofpro-inflammatorycytokines
andpreventedmacrophageandneutrophilinfiltration
intotheinjury
[50]
.Additionally,thepresenceof
hemoglobinamplifiedtheproliferationeffectofLDL
irradiationonlymphocyteculture
[49]
.Hemoglobin
couldcatalyzefreeradicalformationinthepresenceof
hydrogenperoxideasintheFentonreaction
[51]
.LDLat
agivenwavelengthmaypromoteROSformationina
hemoglobinrichenvironment,andthenthegeneration
ofanoxidativeenvironmenthasastronginfluenceon
Tlymphocytes
[52]
.
2Reduced cancer therapy鄄induced
complicationsbyLDL
Notonlydrugresistancecausedbychemotherapy
andmoleculartargetedtherapyisamajorobstacleto
thecurrenttumortreatment
[53
-
55]
,butalsocancer
therapy-inducedcomplicationsareacommonclinical
problem.Inhumanresearches,LDLiswidelystudied
toamelioratecancertherapy-inducedcomplications.
Upperlimblymphedema,whichistheresultofthe
regionalaccumulationofamountsofprotein-rich
interstitialfluidcausedbyimpairedlymphdrainage
[56]
,
isacommoncomplicationofbreastcancersurgery.To
date,researchershavereportedthatLDLisbenefitfor
postmastectomylymphoedema
[57
-
59]
throughpresumably
increasingmicrocirculation
[60
-
61]
toreducetheexcessive
amountsoftissueproteinandfluid,andfinally
improvethelimbperformance.Inparticular,astudy
indicatedthatLDLwasoftenwithinhoursof
irradiationasanefficacytreatmentoflymphedema
[62]
.
However,themolecularmechanismsofLDLin
lymphoedematissueremainelusive.Atthe
microcirculatorylevel,thestimulatory/protective
effectsofLDLisachievedbymodulatingthe
angiogenicfactorproductionbylymphocytes
[63]
and
endothelialcells
[64]
in situ,thentoaccelerate
spontaneousangiogenesis
[65]
.
Oropharyngealmucositis(OM),knownasmost
painfulorallesions
[66]
,isamajorcomplicationofhead-
and-neckoncologictherapy
[67]
.LDLwasconfirmedto
beeffectiveincontrollingofOMcausedbyvarious
cancertherapies
[68
-
71]
.Studieshaveunambiguously
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2017;44(12)
demonstratedthatthemucositispathogenesisare
complexandassociatewithpro-inflammatory
cytokines
[72
-
73]
,microvascularinjury
[74]
,andextracellular
matrixalterations
[75
-
76]
.Silva etal.
[77]
showedthatLDL
increasedthelevelsofIL-10inbloodplasmaand
MMP-2insalivaon7thchemoradiotherapy-induced
OM.StudybyOton-Leite
[78]
demonstratedthatLDL
significantlyreducedsalivaryconcentrationofIL-6,
EGFandVEGFduringradiotherapysession.It
seeminglysuggestedthemechanismofLDL-reduced
theseverityofOMcausedbycancertherapywas
linkedtothemodulationofpro-oranti-inflammatory
cytokines,MMPsorgrowthfactors.Inananimal
modelofOM,studieshavereportedthatLDL
decreasedtheexpressionofCOX-2
[79]
,whichelicitsthe
synthesisofpro-inflammatoryprostaglandinsin
malignantandinflamedtissues,andreducesthe
infiltrationofneutrophilsininflamedtissues
[80]
,thus
furthersupportingtheanti-inflammatoryeffect.
Radiationdermatitis(RD)occursinamajorityof
breastcancerpatientswhoreceiveradiotherapyand
mayexhibitsymptomssuchasredness,itching,
dryness,andpeelingskin
[81]
.DeLand etal.
[82]
showed
thatLDLreducedtheincidenceofskinreactionsin
breastcancerpatientstreatedbyradiotherapy
postlumpectomy.Schindlandco-workers
[83
-
84]
demonstratedthatLDLhealedalong-lasting
radiotherapy-inducedskinulcer.Regardingthe
mechanismofaction,LDLhavebeendemonstratedto
induceneoangiogenesis via theactivationofERK/Sp1
pathway invitro
[64]
and invivo
[83]
,toaccelerate
collateralcirculationandenhancemicrocirculation
[85]
,
thentopossiblyimproveskincirculation
[86]
,andfinally
toreducetissuedamagecausedbyischemia
[87]
.An
alternativeexplanationofLDL-inducedneoangiogenesis
is via ROS
[88]
,whichleadtoincreasethelevelof
HIF-1
[89]
,thenregulatethetranscriptionofVEGF
[90
-
91]
.
Additionally,LDLcouldmodulatecertaincellular
proliferationandmigration
[92
-
94]
,andinducethe
secretionoffibroblastgrowthfactorfamilyinvolvedin
tissuerepair
[95]
.Altogether,thesefindingssuggesteda
beneficialeffectofLDLoncancertherapy-induced
complicationsandpatients’qualityoflifeincancer
patients.
3 Enhancedanti鄄infectionandanti鄄tumor
effectbyLDL
Recently,theeffectofLDL-inducedanti-
infectionwasfurtherconfirmedbyLu etal.
[96]
.They
showedthatLDLenhancedanti-infectionability in
vivo toimprovethemacrophagephagocyticactivity
throughRac1-mediatedsignalingpathway.
Simultaneously,Karunarathne etal.
[97]
showedthat
488-,515-,or595-nmwavelengthlightcouldinitiate
macrophagemigration.Theproductionof
pro-inflammatorycytokines(TNF-琢andIL-1)by
murineperitonealmacrophages invitro and invivo
wasraisedbyLDLaccompaniedwithincreasingthe
abilityofbacterialkilling
[98]
.Inneutrophils,LDLalso
enhancedtheabilitytokill Candidaalbicansvia the
generationofROS
[99]
.Inawoundinfectionmodel,it
wasdemonstratedLDLsignificantlydecreasedthe
incidencesofmicrobialflora(
Staphylococcusaureus
and Bacillussubtilis)comparedwithplaceboburns
[100]
,
andincreasedtheamountofbloodvessels,remodeled
thecollagenmatrix,andmaturedcollagenfibersin
infectedwounds
[101]
.
Theobviousparabolafeaturesofthebiological
effectofLDLoncellshavebeendemonstratedby
severalstudies
[102
-
103]
.Withanincreaseoflightoutput
energy,itsmoderatingactiononcellscanbeincreased
gradually,butwhenthelightoutputenergyexceedsa
certainthresholdvalue,theinhibitioneffectofLDL
emerges
[104]
.AccordingtoLuandcolleagues
[105]
,high
fluence,low-doselight(HF-LDL)wasreportedtokill
tumorcell,leadingtoactivatemacrophagestocreate
animmunememoryresponse.Afewmolecular
mechanismsrevealedthatHF-LDL-inducedapoptotic
tumorcellsenhancedthepro-inflammatorycytokines
(TNF-琢andNO)productioninmacrophage,through
upregulatingNF-资Bactivity
[106
-
107]
.Thosestudiesmay
provideaneffectivetherapeuticapproachtoinducean
antitumorimmuneresponseafterHF-LDLtreatment.
4 Conclusion
Inconclusion,LDLhasstrongevidencesfor
manybeneficialeffectsoninflammatoryreaction,
cancertherapy-inducedcomplications,and
anti-infectionandanti-tumorinanimalmodelsand
humanpatients.Inthisreview,LDL-inducedthose
effectsmainlyinvolve4growthfactors(FGF,EGF,
TGF-茁andVEGF),5interleukins(IL-1,IL-4,IL-6,
IL-8andIL-10),5inflammatorycytokines(PGE2,
COX2,TNF-琢,MMPsandPA)and4immunecells
(macrophages,mastcells,neutrophilsand
lymphocytes).Themediatormoleculesinduced/
upregulatedbyLDLaresummarized(Table1).
However,theunderlyingmechanismsofthoseeffects
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Mediatorclassification Molecules Actions/effects
Growthfactors NGF,GDNF,BDNF,FGF-1/2,bFGF,IGF-1/2,KGF,
PlGF,HGF,PDGF,TGF-
琢
,TGF-
茁
1/2,VEGF
Proliferation/Differentiation/Migration/Chemotaxis/
Angiogenesis/Anti-inflammatory/Extracellularmatrixsynthesis
Anti-inflammatorycytokinesIL-2,IL-4,IL-8,IL-10 Proliferation/Differentiation/Chemotaxis/Angiogenesis/
Immunologicalactivation
Pro-inflammatorycytokinesIL-1
琢
,IL-1
茁
,IL-6,IFN-
酌
,TNF-
琢
,PGE2,COX1,
COX2
Proliferation/Angiogenesis/Migration/Accelerate
inflammation/Immunologicalactivation
Chemokines
MCP-1(CCL2),MIP-1琢(CCL3),MIP-1茁(CCL4),CCR5
Chemotaxis/Immunologicalactivation
Celladhesionmolecules ICAM-1,VCAM-1,CD44,PECAM1,CTGF Proliferation/Differentiation/Angiogenesis/Migration/
Integrinactivation
Cellmatrixproteins MMP1,MMP2,MMP3,MMP9,MMP13,Types
玉
and
域
collagen
Differentiation/Angiogenesis/Regeneration/
Tissueremodeling
Smallmolecules cGMP,cAMP,ATP,GSH,MDA,ROS,Ca
2+
,NO,H
+
Proliferation/Migration/Regulatingcellactivity/
Vasodilatation/Vasoconstriction
Others PA,PTH,Leukotriene,iNOS,LP,ET-1 Proliferation/Degradationoffibrin/Regulatingcellactivity/
Vasodilatation/Vasoconstriction
causedbyLDLarenotcompletelyunderstood.The
precisemolecularmechanismsarestillneededto
furtherexperimentsforpropellingLDLintothe
therapeuticrevolution.
Table1 MediatormoleculesassociatedwithLDL
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follows,whereastheyarenotcomprehensive.Rather,itprovidesinsightintothoseactivitiesassociatedwithLDL.Elementsofthetablewere
developedfromT.Sonis
[108]
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2017;44(12)
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1081· ·

生物化学与生物物理进展 Prog.Biochem.Biophys. 2017;44(12)
低功率光照疗法对机体免疫应答的影响
*
常好才 1) 张真真 2) 刘镭
1)**
(
1) 华南师范大学生物光子学研究院激光生命科学研究所，暨激光生命科学教育部重点实验室，广州
510631
；
2) 中山大学中山医学院人类病毒研究所，广州
510080)
摘要 最近几年，采用红至红外波长(600～1100nm)的低功率光照(low-doselight，LDL)疗法对组织代谢系统、神经系统、
血液循环系统和免疫系统等方面的调节效应已经引起了广泛关注．同时，生物能学和光生物学基础研究的发展推动了低功率
光照在疾病治疗领域的革新．有报道指出，巨噬细胞、肥大细胞、中性粒细胞和淋巴细胞等免疫细胞能响应低功率光照，产
生细胞因子和保护性的蛋白质分子来缓解一些疾病的进程．因此，本文将从分子、细胞和组织水平对低功率光照改善的一些
疾病的免疫学现象及机制进行归纳总结．
关键词 低功率光照，炎症反应，淋巴水肿，口咽黏膜炎，辐射性皮炎，抗肿瘤和抗菌
学科分类号 R454 DOI:10.16476/j.pibb.2017.0275
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14
*
国家自然科学基金
(61361160414,31470072,61405061)
和广东省自然科学基金
(2014A030313419)
资助项目
.
**
通讯联系人
.
Tel:020-85211436, E-mail:liulei@scnu.edu.cn
收稿日期：
2017-07-13
，接受日期：
2017-10-19
1082· ·